Tet1 and Tet2 protect DNA methylation canyons against hypermethylation
DNA methylation is a dynamic epigenetic modification with an important role in cell fate specification and reprogramming. The Ten eleven translocation (Tet) family of enzymes converts 5-methylcytosine to 5-hydroxymethylcytosine, which promotes passive DNA demethylation and functions as an intermedia...
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| Main Authors: | , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
January 19, 2016
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| In: |
Molecular and cellular biology
Year: 2016, Volume: 36, Issue: 3, Pages: 452-461 |
| ISSN: | 1098-5549 |
| DOI: | 10.1128/MCB.00587-15 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1128/MCB.00587-15 Verlag, lizenzpflichtig, Volltext: https://mcb.asm.org/content/36/3/452 
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| Author Notes: | Laura Wiehle, Günter Raddatz, Tanja Musch, Meelad M. Dawlaty, Rudolf Jaenisch, Frank Lyko, Achim Breiling |
MARC
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| 520 | |a DNA methylation is a dynamic epigenetic modification with an important role in cell fate specification and reprogramming. The Ten eleven translocation (Tet) family of enzymes converts 5-methylcytosine to 5-hydroxymethylcytosine, which promotes passive DNA demethylation and functions as an intermediate in an active DNA demethylation process. Tet1/Tet2 double-knockout mice are characterized by developmental defects and epigenetic instability, suggesting a requirement for Tet-mediated DNA demethylation for the proper regulation of gene expression during differentiation. Here, we used whole-genome bisulfite and transcriptome sequencing to characterize the underlying mechanisms. Our results uncover the hypermethylation of DNA methylation canyons as the genomic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts. Canyon hypermethylation coincided with disturbed regulation of associated genes, suggesting a mechanistic explanation for the observed Tet-dependent differentiation defects. Based on these results, we propose an important regulatory role of Tet-dependent DNA demethylation for the maintenance of DNA methylation canyons, which prevents invasive DNA methylation and allows functional regulation of canyon-associated genes. | ||
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